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. 2019 Nov 27;29(4):421–449. doi: 10.1007/s11065-019-09419-2

Table 1.

Study characteristics of included studies

Reference Study design Population N Age at onset (SD) in years Age in study (SD) in years AED use Risk of Bias
Berg et al., 2011, 2014 Prospective CAE 51–59 ESM 5.9 (1.8); VPA 6.4 (1.8) NA ESM 69%, VPA 31% Low
Caplan et al., 2008 Case-control CAE 69 6.15 (2.52) 9.64 (2.49) No AED 12%, Monotherapy 76%- > VPA 51%, ESM 35%, Other 14%, Polytherapy 13% Low
Cerminara et al., 2013 Case-control CAE 24 NA NA VPA 18, LEV 4, LTG 1, VPA + LTG 1 Moderate
Cheng et al., 2017 Case-control CAE 43 ≤5: n = 14; >5 29 9.5 (2.6) No AED 7%, Monotherapy 72%, Duotherapy 21% Low
Conant et al., 2010 Case-control CAE 16 4.5–8 8.0 (1.3) No AED 6, VPA 10, VPA + ESM 1 Low
Conde-Guzon & Cancho-Candela, 2012 Case-control AE 34 5.1 (1.2) 8.7 (1.26) 100% VPA Low
Covanis et al., 1992 Retrospective AE 124 2.5–13.5 NA Moderate
D’Agati et al., 2012 Case-control CAE 15 8.8 (1.74) 11.46 (2.23) VPA 100% Moderate
Fastenau et al., 2009 Prospective AE 38 6–14 NA NA Low
Franzoni et al., 2015 Retrospective AE drug-resistant 92 5.33 3y minimal follow-up time Polytherapy 100%, >3AED’s 47%, >5 AED’s 53% Low
Gencpinar et al., 2016 Case-control CAE 69 3–6; n = 14, ≥7 n = 5 12.22 (2.46) Monotherapy 73.7%, Duotherapy 26.3%, Tripletherapy 26.3% Moderate
Guerrini et al., 2015 Case-Control CAE 82 6.28 (2.5) 9.7 (1.78) NA Low
Henkin et al., 2003, 2005 Case-control AE 12 7.2 14.4 (1.83) VPA 100% Moderate
Kernan et al., 2012 Case-control CAE 31 6 (2) 9 (2) No AED 6%, Monotherapy 68%, Polytherapy 26% Low
Levav et al., 2002 Case-control CAE 28 5.6 (2–16) 14.0 (10.5) No AED 18, Monotherapy 7, Polytherapy 3 Low
Lopes et al., 2013, 2014 Case-control CAE 30 6.83 (2.32) 9.93 (2.54) No AED 13%, Monotherapy 73%, Duotherapy 13% Low
Masur et al., 2013; Shinnar et al., 2017 RCT CAE 446

≥6 years of age n = 336

<6 years of age n = 110

Pre-treatment analysis

(=max. 1 week after start AED)

After randomization: ESM 35%, LTM 33%, VPA 32% Low
Mostafa et al., 2014 Cross-sectional CAE 10 8.4 (1.9) 13 (4.1) VPA 80%, LTG 20% Low
Nolan et al., 2004 Prospective CAE 13 5.5 (2.0) 9.5 (2.3) Monotherapy 48%, Polytherapy 62% Moderate
Oostrom et al., 2003 Prospective CAE or JAE 10 NA 9.2 (1.9) 100% AED not specified Moderate
Pavone et al., 2001 Case-control AE 16 5.3 9.2 (3) ESM 2, VPA 11, ESM + VPA 3 Low
Schraegle et al., 2016 Cross-sectional CAE 30 4.83 (1.89) 11.1 (2.95) Monotherapy 16%, Polytherapy 46.7% Low
Sinclair & Unwala, 2007 Retrospective AE 80 7.5 (2.7) 13.9 (3.2) NA Moderate
Siren et al., 2007 Case-control CAE 9, JAE 1 10 3.0–11.8 8.2, 5.5–14.5 VPA 4, ESM 5, VPA+ESM 1 Low
Urena-Hornos et al., 2004 Retrospective AE 49 7.93 10 days-13 years follow up Monotherapy VPA 78%‡ Moderate
Vanasse et al., 2005 Case-control AE 10 5.17 (2.26) 10.13 (1.69) Monotherapy 5, Polytherapy 5 Moderate
Vega et al., 2010 Case-control CAE 38 6.9 (2.8) 10.5 (2.3) No AED 13.2%, Monotherapy 63.2%, Duotherapy 21.1%Polytherapy 2.6% Low
Verrotti et al., 2011 Retrospective AE before age of 3 40 2.2 (0.59) 8.19 No AED 2, VPA 26, LTG 1, LEV 1, ESM 3, VPA- > CLB 1, VPA->ESM 2, VPA- > LEV 1, VPA- > LTG 1, VPA->ESM 1, VPA- > CLB 1 Low
Wirrell et al., 1996 Retrospective CAE 60 5.7 (2.8) 20.4 (4.2) No AED 47, VPA 9, VPA + LTG 1, LTG 1 VPA+ESM 1, ESM + LTM + CBM 1 Moderate

a May contain overlapping patients, however reports on neuropsychological test results did not overlap ‡ Refer to original paper

AE, Absence Epilepsy; AED, Anti-Epileptic Drug; CAE, Childhood Absence Epilepsy; CBM, Carbamazepine; CLB, Clobazam; ESM, Ethosuximide; JAE, Juvenile Absence Epilepsy; LEV, Levetiracetam; LTG, Lamotrigine; N, number of patients; NA, Not available; RCT, Randomized Clinical Trial; SD, Standard Deviation; VPA, Valproic Acid